1. The nature and magnitude of the problem Tetanus is an
acute disease induced by an exotoxin of the tetanus bacillus, which
grows anaerobically at the site of an injury. Occurrence is worldwide,
but is most frequently encountered in densely populated regions
in hot, damp climates with soil rich in organic matter. The true
incidence of tetanus is not known, but is estimated to be
between 500,000 to one million cases per year worldwide. The majority
of cases occur in developing countries, with 50% of those cases
occurring in neonates. The survey (November 2001) of National Statistical
Center confirmed the assumption that neonatal tetanus is
a major public health problem in the Lao People's Democratic Republic
and showed an estimated neonatal tetanus mortality rate of
between 8 and 10 per 1000 live births. This is partly because the
coverage of antenatal care is very low and only 31% of pregnant
women are immunized with tetanus toxoid, and partly because trained
personnel assist fewer than 10% of deliveries. Based on these findings
a national plan of action was developed towards maternal and neonatal
tetanus elimination by 2005.
2. Infectious agent C. tetani is a slender, gram-positive,
anaerobic rod that may develop a terminal spore, giving it a drumstick
appearance. The organism is sensitive to heat and cannot survive
in the presence of oxygen. The spores, in contrast, are very resistant
to heat and the usual antiseptics. They can survive autoclaving
at 121°C for 10-15 minutes. The spores are also relatively resistant
to phenol and other chemical agents. The spores are widely distributed
in soil and in the intestine and feces of horses, sheep, cattle,
dogs, cats, rats, guinea pigs, and chickens. Manure-treated soil
may contain large numbers of spores. In agricultural areas, a significant
number of human adults may harbor the organism. The spores can also
be found on skin surfaces and in contaminated heroin. There is no
laboratory findings characteristic of tetanus. The diagnosis is
entirely clinical and does not depend upon bacteriologic confirmation.
C. tetani is recovered from the wound in only 30% of cases, and
can be isolated from patients who do not have tetanus. Laboratory
identification of the organism depends most importantly on the demonstration
of toxin production in mice.
3. Reservoir Organisms are found primarily in the soil and intestinal
tracts of animals and humans.
4. Mode of transmission
Transmission is primarily by contaminated wounds (apparent and inapparent).
The wound may be major or minor. In recent years, however, a higher
proportion of cases had minor wounds, probably because severe wounds
are more likely to be properly managed. Tetanus may follow elective
surgery, burns, deep puncture wounds, crush wounds, otitis media
(ear infections), dental infection, animal bites, abortion, and
pregnancy. In a few cases the portal of entry is either trivial
e.g. rose thorn in the finger. Tetanus, however, does not occur
only in classic "puncture" wounds. Between 1991 and 1994, no portal
of entry was detected in 22% of the cases reported to the CDC (5).
Therefore, relying on "proper wound management" alone will not effectively
eliminate tetanus in adults. Patients of all ages must continue
to be adequately immunized.
5. Incubation period
The incubation period, which is the time between the introduction
of spores in the body and the first clinical symptoms, varies from
1 day to several months (usually 3-21 days). Most cases occur within
14 days. The duration of incubation, as well as the interval between
first symptoms and generalized spasms (the period of onset), determine
the severity of the disease and therefore the prognosis. In general,
the shorter the period from injury to onset of symptoms and the
shorter the time interval between symptoms and spasms, the more
severe the tetanus will be.
6. Period of communicability Tetanus is not contagious from person to person. It is the
only vaccine-preventable disease that is infectious, but not contagious.
7. Susceptibility and resistance Susceptibility is general. Active
immunity is induced by tetanus toxoid and persists at least 10 years
after full immunization. Infants of actively immunized mothers acquire
passive immunity that protects them from neonatal tetanus. Recovery
from tetanus may not result in immunity; second attacks can
occur. Primary immunization is indicated after recovery. The disease
normally affects unimmunised or partially immunized people, and
risk increases with age. Titres of antibodies to tetanus are inadequate
to ensure protection in 50% of people older than 65 years. Whenever
a previously-immunized individual sustains a potentially dangerous
wound, a booster of toxoid should be injected.
8. Epidemics
In rare instances, outbreaks of tetanus among injecting drug
users have occurred.
9. Pathogenesis
C. tetani usually enters the body through a wound. In the
presence of anaerobic (low oxygen) conditions, the spores germinate.
The toxin is produced during cell growth, sporulation and lysis.
It migrates along neural paths from a local wound to sites of action
in the central nervous system. Part of toxins, including tetanospasmin,
is disseminated via blood and lymphatics. Toxins act at several
sites within the central nervous system, including peripheral motor
end plates, spinal cord, brain, and sympathetic nervous system.
Tetanus toxin interferes with release of neurotransmitters, blocking
inhibitor impulses. This leads to unopposed muscle contraction and
spasm. Seizures may occur, and the autonomic nervous system may
also be affected. Incubation may vary from as short as 24 h to as
long as many months. This interval may be a reflection of the distance
the toxin must travel within the nervous system and the quantity
of toxin released. Tetanus toxin is one of the three most poisonous
substances known, the other two being the toxins of botulism and
diphtheria. Tetanus toxin is produced in vitro in amounts up to
5 to 10% of the bacterial weight. Because the toxin has a specific
affinity for nervous tissue, it is referred to as a neurotoxin.
The toxin has no known useful function to C. tetani. Why the toxin
has a specific action on nervous tissue, to which the organism naturally
has no access, may be an anomaly of nature.
10. Clinical features
Rapid case identification of tetanus is important clinically because
hospitalization may be required.
Case definition: Acute onset of hypertonia and/or painful muscular
contractions (usually of the muscles of the jaw and neck) and generalized
muscle spasms without other apparent medical cause. Tetanus may
be localized at the site of injury resulting in local pain and rigidity
often with a low mortality. When local tetanus follows head, facial
injuries or chronic otitis media, cephalic tetanus can occur which
is a local variant (often involving cranial nerves particularly
the seventh cranial nerve) but has a higher mortality. Both of these
may progress to the more common generalized form, which may present
with pain, stiffness, rigidity, trismus (rigidity of the masseter
muscles), dysphagia, opisthotonus and spasms. The clinical pattern
of generalized tetanus consists of severe painful spasms and rigidity
of the voluntary muscles. The characteristic symptom of "lockjaw"
involves spasms of the masseter muscle. It is an early symptom,
which is followed by progressive rigidity and violent spasms of
the trunk and limb muscles. Spasms of the pharyngeal muscles cause
difficulty in swallowing. Death usually results from interference
with the mechanics of respiration. On the basis of clinical findings,
different forms of tetanus have been described. Generalized tetanus
is the most common type (about 80%) of reported tetanus. The disease
usually presents with a descending pattern. The first sign is trismus
or lockjaw, followed by stiffness of the neck, difficulty in swallowing
(spasms of the pharyngeal muscles), and rigidity of abdominal muscles.
Other symptoms include a temperature rise of 2°-4°C above normal,
sweating, elevated blood pressure, and episodic rapid heart rate.
Spasms may occur frequently and last for several minutes. Spasms
are usually worst during the first 2 weeks with autonomic instability
following some days after the onset of spasms and often peaking
during the second week of the disease. Rigidity may continue after
the spasms and autonomic disturbances have started to improve. Spasms
continue for 3-4 weeks. Complete recovery may take months. Local
tetanus is an uncommon form of the disease, in which patients have
persistent contraction of muscles in the same anatomic area as the
injury. These contractions may persist for many weeks before gradually
subsiding. Local tetanus may precede the onset of generalized tetanus,
but is generally milder. Only about 1% of cases are fatal. Cephalic
tetanus is a rare form of the disease, occasionally occurring with
otitis media (ear infections) in which C. tetani is present in the
flora of the middle ear, or following injuries to the head. There
is involvement of the cranial nerves, especially in the facial area.
Neonatal tetanus is a form of generalized tetanus that occurs in
newborn infants. It develops in children born to inadequately immunized
mothers, frequently after unsterile treatment of the umbilical cord
or its stump. Neonatal tetanus is common in some developing countries
(estimated >270,000 deaths worldwide per year). Maternal tetanus
defined as tetanus occurring during pregnancy or within 6 weeks
after any type of pregnancy termination. It includes postpartum
or puerperal tetanus resulting from septic procedures during delivery,
postabortal tetanus resulting from septic abortion and tetanus incidental
to pregnancy, resulting from any type of wound during pregnancy.
12. Complications.5 Laryngospasm (spasm of the vocal cords) and/or
spasm of the muscles of respiration leads to interference with breathing.
Aspiration pneumonia is a common late complication of tetanus, found
in 50%-70% of autopsied cases. Fractures of the spine or long bones
may result from sustained contractions and convulsions. Hyperactivity
of the autonomic nervous system may lead to hypertension and/or
an abnormal heart rhythm. Nosocomial infections are common because
of prolonged hospitalization. Secondary infections may include sepsis
from indwelling catheters, hospital-acquired pneumonias, and decubitus
ulcers. Pulmonary embolism is particularly a problem in drug users
and elderly patients. Death. In recent years, tetanus has
been fatal in approximately 11% of reported cases. Mortality of
this condition is usually due to autonomic dysfunction or nosocomial
infections especially pneumonias. Cases most likely to be fatal
are those occurring in persons age >60 years (18%, and unvaccinated
persons (22%). In about 20% of tetanus deaths, no obvious pathology
is identified and death is attributed to the direct effects of tetanus
toxin. The reduction in mortality over the last three decades is
due largely to the use of exceptionally heavy sedation rather than
to muscle paralysis to control the spasms and prevent lifethreatening
effects of autonomic overactivity. The reduction in mortality has
also been achieved by attention to detail and the improved care
of long-term ITU patients. There is huge discrepancy between the
incidence and related morbidity and mortality between the developed
and developing world with over 400 000 neonatal deaths a year. 13.
Differential diagnosis The differential diagnosis includes dystonic
drug reactions, meningitis/encephalitis, rabies, tetany, strychnine
poisoning, facial pathology (jaw stiffness, dental abscess). In
neonates, one also has to exclude hypocalcaemia, hypoglycaemia,
meningitis and meningoencephalitis, seizures due to other aetiologies.
5

14. Clinical assessment
Classification of grades of severity of tetanus
Mild The mild forms had long incubation periods and trismus (lockjaw),
neck stiffness and risus sardonicus were the only symptoms. There
were no convulsions and no general toxic disturbances such as hyperpyrexia.
The prognosis was generally good with no case fatality Moderate
Moderate forms are characterized by generalized spasmodic contractions
with opisthotonos, but they are only provoked by external stimuli
such as skin punctures, nasopharyngeal suction, loud noise or intense
light. There is abdominal pain and backache, but no fever. The prognosis
is less good. Severe In the severe forms, with short incubation
periods, generalized convulsions are spontaneous and long-lasting,
with frequent episodes of apnea, cyanosis and asphyxia. There are
central nervous system disturbances such as hyperpyrexia, tachycardia
or cardiac arrest. Even with specialized intensive care including
respiratory assistance, the prognosis is extremely poor.
15. Case management
The goals of therapy are to eliminate the source of toxin, neutralize
unbound toxin, prevent muscle spasm, and provide support, especially
respiratory support until recovery. Prompt administration of TT
and TIG may decrease the severity of the disease. Maintenance of
the airway The critical factor in patients with tetanus is to maintain
a patent airway. Laryngospasm occurs commonly as part of generalized
spasms and can often be precipitated by oral secretions or manipulations.
Due to the inability to swallow, secretions are a problem and patients
are unable to clear them adequately. These can lead to laryngospasm.
Fatal laryngospasm has been recorded before any generalized muscular
spasm has occurred. When the patient develops spasms, which are
not controlled by a small dose of diazepam and dysphagia is present,
they should have the airway protected by intubation and early tracheostomy
due to the predictable long course of these patients. It is important
to intubate early rather than take the chance of the patient developing
laryngospasm. Due to the tendency to laryngospasm on any stimulation
these patients should never be intubated without sedation and a
muscle relaxant (general anaesthesia). The trismus always relaxes
with succinylcholine which is useable at this stage, but not later,
once prolonged disuse has taken place. Sympathetic overactivity
Sympathetic overactivity remains the major cause of death in patients
with tetanus once the early deaths from airway obstruction and the
deaths from respiratory failure have been eliminated. The syndrome
of sympathetic overactivity results in a tachycardia (or occasionally
a profound bradycardia), marked fluctuation in blood pressure (both
hypotension and hypertension), excessive salivation and sweating.
This fluid loss may result in large fluid losses and clinically
significant dehydration. The effect on the heart can give rise to
cardiomyopathy, ECG changes, dysrrythmias and myocardial infarction.
Basal catecholamine concentrations may be increased 10-fold with
greater increase in sympathetic neuronal activity compared with
adrenal medullary activity (noradrenaline more marked than adrenaline).
That is why treatment by paralysis alone is not logical as this
treats only the somatic system and leaves sympathetic stimulation
untreated. If one uses large doses of hypnotics sufficient to cause
general anaesthesia, both the somatic and sympathetic nervous system
will be inhibited centrally.
16. Treatment
I. Supportive Tracheostomy
A tracheostomy should be done under general anaesthesia in an operating
theatre. Although percutaneous tracheostomy is now a routine technique
in many intensive care units and may have certain advantages, it
may not be available in developing countries. Deep venous thrombosis
prophylaxis This is important as thromboembolic complications are
an important cause of mortality due to prolonged immobility, dehydration
and sympathetic overdrive. Subcutaneous heparin 5000 IU 8-hourly
and graded stockings are recommended. intravenous injection of diazepam
or might need to be paralysed to enable adequate physiotherapy.
However, regular tracheal suctioning is essential to prevent atelectasis,
lobar collapse and pneumonia. Immobility considerations are important
and passive range-of motion exercises must be instituted to maintain
muscle strength and prevent deformities and contractures. Splints
may be required. Physiotherapy and occupational therapy would also
be required during the rehabilitation phase. Ventilation Many patients
with the generalized form of tetanus will require intubation and
ventilation both for airway protection and respiratory support particularly
if their forced vital capacity is less than 1200 ml (normal 4000
- 5000 ml) and their peak negative inspiratory pressure is less
than 35 cm H2O (normal 75 to 100 cm H2O). Patients should all receive
intermittent positive pressure ventilation (IPPV) with at least
5 cm H2O of positive end expiratory pressure (PEEP) provided there
is no contraindication to PEEP. In the later stages of the disease
other modes of ventilation may be introduced to allow an appropriate
component of spontaneous ventilation (synchronized intermittent
mandatory, continuous positive airway pressure or biphasic positive
airway pressure ventilation). This allows reduction of sedation
(if the primary pathology is improving), may minimize muscle wastage
and may reduce the likelihood of critical illness neuropathies or
myopathies. Physiotherapy and occupational therapy These patients
need regular chest physiotherapy and often require a bronchodilator
in the nebulizer. Due to the excessive secretions, both oral and
bronchial, they are particularly prone to develop nosocomial pneumonias
and areas of atelectasis. It is important to try and reduce the
amount of secretions, which accumulate between the vocal cords and
the tracheostomy cuff as this may predispose to lower respiratory
infection due to microaspiration (continuous 'vocal aid' suctioning
may help in this regard). Patients might require an additional intravenous
injection of diazepam or might need to be paralysed to enable adequate
physiotherapy. However, regular tracheal suctioning is essential
to prevent atelectasis, lobar collapse and pneumonia. Immobility
considerations are important and passive range-ofmotion exercises
must be instituted to maintain muscle strength and prevent deformities
and contractures. Splints may be required. Physiotherapy and occupational
therapy would also be required during the rehabilitation phase.
Intravenous lines A central line inserted under aseptic techniques
must be used because of the intravenous penicillin (although there
is a shift away from the use of penicillin to other antibiotics
as will be mentioned later), which is usually given for the first
10 days. As soon as this line is no longer needed it should be removed,
as it is just another source of infection. Try not to have any intravenous
lines once the autonomic instability and spasms are well controlled
on nasogastric tube medication. Fluid balance This is important
due to increased losses from sweating, salivation and GIT losses.
Being fluid replete may help to manage the autonomic instability.
Acute renal failure is fairly common in generalized tetanus and
may be due to the fluid shifts, cardiovascular instability and rhabdomyolysis.
Feeding A nasogastric tube (NGT) should be passed on admission and
can be used immediately for drugs provided there is no ileus and
nasogastric feeds can be commenced as soon as possible. The regular
tube feeds with additional supplementation with vitamins and trace
elements must be given. The daily caloric requirements in well-controlled
tetanus will be within 15% of the predicted requirements. Early
enteral feed is recommended. If this is not possible then total
parenteral nutrition should be commenced early. Some units would
advocate prophylaxis for stress ulcers if the patient is not being
fed enterally and this may be appropriate during the period of high
sympathetic outflow. Expert nursing care A few points in the nursing
care should be carefully verified:
(a) Meticulous tracheostomy care using low-pressure cuff tracheostomy
tubes to try and prevent tracheal stenosis. These must be inflated
correctly against a manometer.
(b) Tracheostomy securing tapes to be tied tightly with a 2-finger
space only.
(c) The patient who is unable to breathe on his/her own, either
because of heavy sedation or if he/she is paralysed, must have someone
specialling him/her continuously.
(d) Use a constant-volume ventilator with all alarms correctly set.
(e) Meticulous care of pressure areas to prevent the development
of bedsores.
(f) Routine oropharyngeal care (regular suctioning, dental suction,
'vocal-aid' suctioning).
(g) Routine ocular care (all heavily sedated patients).
(h) Pay particular attention to drip sites, tracheostome, urinary
catheter and nasogastric tube to minimize the incidence of infection.
The condition and the treatment may immunosuppress these patients
making them more prone to infection. Strict aseptic technique and
constant nursing surveillance to recognize life-threatening situations
early are essential.
(i) Slight external stimuli such as noise or tactile stimulation
can trigger muscle spasms and autonomic instability. The environment
therefore needs to be kept as quiet and dark as possible. The nurses
can co-ordinate care and contact activities by personnel from all
disciplines in an effort to decrease incidence of stimulation and
maintain a calm environment.
(j) Psychological care for both the patient and relatives is important
and may best be co-ordinated and addressed by the nursing team who
spend the most time with the patient and family. They may then bring
it to the attention of the rest of the multidisciplinary team.
(k) The clinical course of tetanus is often unpredictable (particularly
if there are associated complications of prolonged critical illness
including ventilator associated pneumonias, generalized sepsis,
gastrointestinal haemorrhage, thromboembolic complications). All
these patients should therefore be closely monitored throughout
their illness and for a period of recuperation thereafter. After
the initial airway and autonomic problems it is often the level
of nursing care of these long-term patients which dictates the morbidity
and mortality.
II. Specific Surgical debridement
The patient should be carefully examined for a wound. Early surgical
debridement is an essential part of the therapy as this obligate
anaerobe requires devitalized tissue, which is potentiated by the
production of Tetanolysin, a substance which disrupts cell membranes
damaging viable tissue. It should include wide excision of the site
of infection under general anaesthesia. It can be done under general
anaesthesia at the same time as the tracheostomy. If the tetanus
progresses (worsening autonomic instability and spasms) for more
than 5-10 days following institution of adequate therapy, further
exploration and debridement of the original wound should be undertaken
as foreign bodies may frequently be missed on initial exploration.
III. Facilitative Heavy sedation Diazepam is the mainstay of the
hypnotic drugs. It has a wide margin of safety, can be given orally
(via a nasogastric tube), rectally or intravenously and is a sedative,
anticonvulsant and a muscle relaxant. It is also cheap and available
in most parts of the world. It does have a long cumulative half-life
and has active metabolites. Initially, it can be given intravenously
in 10 mg increments until the patient is stabilized. In patients
with severe tetanus an infusion of thiopentone sodium may be necessary
in addition to the diazepam to achieve adequate control. As soon
as the patient can receive oral medications via a nasogastric tube
diazepam should be given orally as should all the other drugs. Diazepam
is then given as required and doses greater than 1 g/day may be
necessary. It is initially started in a dosage schedule of approximately
20 mg 4}6-hourly and if this is insufficient the time interval between
doses is reduced until the patient is receiving diazepam in doses
that may exceed 100 mg 2-hourly. At this stage, if further sedation
is still necessary, the dose of diazepam can be further increased
but barbiturates and/or a phenothiazine should be added in addition.
Chlorpromazine is a useful sedative with alphaadrenergic and anticholinergic
effects. Morphine may be a useful addition for its sedation properties,
which may not compromise cardiac performance. However, the opioids
may contribute towards unwanted gastrointestinal effects (e.g. gastroparesis,
prolonged ileus or constipation) which one should try to avoid or
may need further management should they occur. When necessary, we
have given 240 mg phenobarbitone 8-hourly orally (alternatively
up to 600 mg of amylobarbitone over 24 h), 1 g diazepam over 24
h orally and 150 lg clonidine 8-hourly orally. In addition, occasional
thiopentone infusions have been necessary. It is important, however,
to space the doses of different drugs and try to give one drug at
a time to avoid hypotension. Dosage of hypnotics is obviously far
in excess of what a normal patient would tolerate and important
signs to watch for overdosage are hypothermia and hypotension. This
occurs particularly when the effects of the tetanus are wearing
off. With the institution of therapy, the clinical severity of the
disease should not progress and its severity may then be assessed
by the amount of sedative drugs required. The tetanus usually runs
its self-limiting, natural course within 3}4 weeks and the sedatives
are usually reduced at this time after which it may take a week
or more for the patient to wake sufficiently to be considered for
extubation. If the spasms or autonomic instability recur then the
patient is resedated for a further week and then weaning is attempted
again. Even with the long-acting benzodiazepines (diazepam), one
should look for signs of withdrawal (more of a problem with the
shorter-acting benzodiazepines like midazolam) and the dose may
need to be reduced slowly. Muscle relaxants Muscle relaxants are
now used only intermittently to control severe spasms or to enable
adequate physiotherapy. They have no beneficial effect towards the
autonomic instability and make it difficult to assess the signs
of anaesthesia when the patient is paralysed. Muscle relaxants that
may be used include pancuronium, vecuronium, rocuronium and atracurium.
Pancuronium and atracurium may, however, reduce haemodynamic stability
due to catecholamine effects or histamine release. It must be remembered
that problems have been reported with the extended use of non- depolarizing
muscle relaxants. Agents like dantrolene and baclofen have been
used with varying success. Heavy sedation alone may provide adequate
neuromuscular relaxation. Sedation with propofol may allow control
of spasms and rigidity without additional relaxant with appropriate
effects noted on EMG. With our heavy sedation regimen described
above, we have also found little need for neuromuscular blocking
agents. Management of autonomic disturbance Sedation, which is useful
for controlling spasms and rigidity, is also the first step in reducing
autonomic instability and is essential in the management of tetanus.
If the resting heart rate is more than 120 beats/min with adequate
sedation, propranolol may be given in a starting dose of 10 mg twice
daily by mouth. Concerns about beta-blockade and sudden death have,
however, been raised. The use of of alpha-blockade should be avoided
because it complicates the management without adding any positive
contribution to the therapy. Alpha-blocking agents may have a small
role if a patient has an unopposed vasoconstrictor response to beta-blockade.
Labetalol (combined alpha- and beta-blockade) or the use of the
short-acting agent esmolol may have a role although it is expensive
and does not decrease catecholamine levels. Other components of
autonomic instability may be treated with magnesium, which is cheap
and reduces both catecholamine release and receptor responsiveness
with few side-effects in the ventilated patient. Magnesium sulphate
should be given as a 5 g loading dose over 20 min and then followed
by an infusion of between 2 and 3.5 g/h for up to 4 weeks in ventilated
patients. Appropriate monitoring of both Mg2` and Ca2` levels is
required.
17. Medication Anti-tetanus serum About 1500 - 6000 units
of human tetanus immunoglobulin (HTIG) should be given intravenously.
A dose of 500 units may be as effective as the larger doses. Should
this not be available the patient should receive 40 000 units of
antitetanus serum (horse) intramuscularly and 40 000 units intravenously
following a test dose as there is a 20% incidence of anaphylactic
reactions. If the patient reacts to the test dose the anti-tetanus
serum can be skipped. The true value of this therapy has not been
validated and the rapidity with which the tetanospasmin fixes irreversibly
to neural tissue may limit its value. The benefit of intrathecal
HTIG is, as yet, not confirmed. Antibiotics Patients should be treated
with intravenous benzylpenicillin in a dosage of 1megaunit 6-hourly.
Metronidazole 500 mg intravenously 8-hourly (or rectal after a few
days) is a safe and adequate alternative and in a prospective, open,
non-randomized clinical trial those patients who received metronidazole
had a lower mortality and a shorter hospital stay. Erythromycin,
tetracycline, vancomycin, clindamycin, doxycycline and chloramphenicol
would be alternatives to penicillin and metronidazole if those were
unavailable or unusable in individual patients. Patients who have
tetanus often have a pyrexia which might be as high as 40 C and
this may be due to pyrogens, metabolic stimulation, muscular activity
caused by the tetanus or due to toxin effects on the medullary centres
of the brainstem. It can be expected and need not necessarily be
indicative of an ongoing infection. Tetanus itself induces no immunity
and these patients all require active immunization with tetanus
toxoid. (Toxoid 0.5 ml by intramuscular injection on discharge with
a follow-up booster at 2 months and again at 6 months.)
18. Prevention
Active immunization A booster should follow three intramuscular
injections of tetanus toxoid every 7 years. Alum absorbed tetanus
toxoid is very effective at preventing tetanus with a failure rate
of 4 in 100 million immunocompetent individuals. If a wound has
the possibility of being contaminated with dirt, faeces, soil or
saliva or there is a lot of devitalized tissue then HTIG should
be considered (250 units by intramuscular injection). Neonatal tetanus
can be prevented by immunization of women during pregnancy. In most
developing countries, routine immunization in infancy was not implemented
until the mid 1980s. Therefore, many women of childbearing age from
the developing countries may be susceptible to tetanus. For
previously unimmunized women living in the developing countries,
the World Health Organization (WHO) recommends five doses of tetanus
toxoid in order to ensure long- term immunity. The first two doses
given 1 month apart provide short-term immunity. These first two
doses provide 80% protection to the newborn; the third dose increases
the protection for the fetus to 95% (3). The third dose of tetanus
(scheduled 6–12 months after the second and, therefore, not commonly
given in pregnancy) induces a durable immunity for the woman lasting
a minimum of 5 years, the fourth dose prolongs immunity for 10 years,
and the fifth dose prolongs immunity for at least 20 years (4).
In the United States, the ACIP recommends a three-dose primary series
for unimmunized individuals or for those without documentation,
followed with a booster dose every 10 years.